Comparative genomics reveals insights into characterization and distribution of quorum sensing-related genes in Shewanella algae from marine environment and clinical sources.

Shewanella algae is not only the most commonly reported species in Shewanella human infections but also capable to inhabit a wide variety of habitats. Although there is evidence that quorum sensing is associated with bacterial adaptation to changing environmental conditions, little is known of the quorum sensing system in S. algae. In this study, we conducted the whole genome sequencing of S. algae strains and applied comparative genomics to reveal the core genome. Genes related to the quorum sensing system were identified by integrated bioinformatics analysis. S. algae harbor genes involved in all three main types of autoinducer systems. This study provides insights into the quorum sensing systems in S. algae, which might be valuable in the future study of cell behavior in S. algae.

Comparative Genomics Reveals Pathogenicity-Related Loci in Shewanella algae.

Shewanella algae is an emerging marine zoonotic pathogen and accounts for considerable mortality and morbidity in compromised hosts. However, there is scarce literature related to the understanding of the genetic background of virulence determinants in S. algae. In this study, we aim to determine the occurrence of common virulence genes in S. algae using whole-genome sequence and comparative genomic analysis. Comparative genomics reveals putative-virulence genes related to bile resistance, chemotaxis, hemolysis, and motility. We detected the existence of hlyA, hlyD, and hlyIII involved in hemolysis. We also found chemotaxis gene cluster cheYZA operon and cheW gene. The results provide insights into the genetic basis underlying pathogenicity in S. algae.

Characterization of the bidirectional promoter region between the human genes encoding VLCAD and PSD-95.

Bidirectional promoters are widely known among lower organisms but rare in mammals. A shared promoter between the two human genes encoding very long chain acyl-CoA dehydrogenase (VLCAD) and postsynaptic density protein 95 (PSD-95) is an ideal model to investigate bidirectional transcription in mammals. VLCAD associates with the inner mitochondrial membrane and catalyzes the initial step in mitochondrial long-chain fatty acid beta-oxidation. PSD-95, a component protein of the PSD, plays an essential role in clustering the transmembrane proteins in synaptic membranes. Interestingly, the human genes encoding VLCAD (ACADVL) and PSD-95 (DLG4) are adjacently located in the head-to-head orientation on chromosome 17p. The transcribed regions of the two genes overlap, while the two transcription start sites stand approximately 220 bp apart. To analyze the common transcriptional control region shared by the two genes, we generated serial promoter partial deletion constructs using firefly luciferase as the reporter gene. Our results showed that the essential promoter activity of PSD-95 is carried within an approximately 400-bp region, which covers the entire approximately 270-bp minimal promoter of VLCAD. The results from di-(2-ethylhexyl) phthalate (DEHP)-treated HepG2 cells revealed that the minimal VLCAD promoter is able to up-regulate VLCAD expression in response to DEHP treatment. Site-directed mutagenesis experiments showed that a mutated activator protein 2-binding site markedly reduced the transcriptional activity of both promoters and abolished the minimal VLCAD promoter's response to DEHP treatment.